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Some Physiological and Clinical Aspects of Puberty* H Arch Dis Child: first published as 10.1136/adc.48.3.169 on 1 March 1973. Downloaded from Review article Archives of Disease in Childhood, 1973, 48, 169. Some physiological and clinical aspects of puberty* H. K. A. VISSER From the Department of Paediatrics, Medical Faculty and Academic Hospital, Sophia Children's Hospital and Neonatal Unit, Rotterdam, The Netherlands Puberty is usually taken to be the process of embryonic life. Cytogenetics, experimental embry- maturation of the sexually immature child into the ology and endocrinology, steroid biochemistry, sexually mature adolescent, while the term adoles- and clinical medicine have contributed to the rapid cence has been used to describe that period of increase in our knowledge during the past decades. human development when secondary sex charac- Much of our information has been derived from teristics have appeared completely but full maturity animal experiments and the results of these experi- has not been reached. Recently psychologists and ments very often, but not always, can be applied child psychiatrists have been using the term adoles- to the human. cence particularly to refer to the emotional and behavioural development and the changes in social Early differentiation of gonads and genital copyright. interaction during this period of life. In this organs. The structure of the undifferentiated review we shall use, as Tanner (1962), the words gonad is identical in male (XY) and female (XX) puberty and adolescence without distinction. embryos until the 7th week. In the 7th week in This review will emphasize physiological rather the XY-embryo the medullary tissue of the un- than clinical aspects of puberty. Several excellent differentiated gonad begins to develop in a fetal books and review papers on the subject are available testis. About two weeks later in the XX-embryo (Tanner, 1962, 1969, 1970; Falkner, 1966; Marshall the cellular cortex starts to differentiate in a fetal and Tanner, 1968; Donovan and van der Werff ovary. Interstitial cells of Leydig are visible at http://adc.bmj.com/ ten Bosch, 1965; van der Werff ten Bosch, 1965; about 8 weeks and it is generally accepted that their Hubble, 1969; Prader, 1971; Gold and Douvan, secretions are responsible for further male differen- 1969), but adolescent medicine has been a long tiation of genital ducts and external genital organs. neglected field ofmedicine on the borderline between The fetal testis acts in three ways: it induces paediatrics and internal medicine. It should not development of the external genital organs, it be regarded as a new specialty, but be integrated stimulates differentiation of the Wolffian duct, into paediatrics. Studying the anatomy and physio- and it inhibits differentiation of the Miullerian duct. on September 26, 2021 by guest. Protected logy of adolescence, the paediatrician will gain more Our knowledge in this field is mainly based on the insight into the pathology of this period of life, and brilliant animal experiments of Jost (1958). Induc- he will understand better the problems of boys and tion of the development of the external genital girls in the period between childhood and adult organs is an androgenic hormonal effect that can life. be reproduced by administering testosterone. Physiologically the substance most probably respon- Sexual maturation and differentiation during sible is testosterone, secreted by the Leydig cells adolescence of the fetal testis. Jost's experiments have shown Maturation of gonadal secretory function and the that male duct differentiation is promoted by a development of secondary sex characteristics during factor which is secreted by the fetal testis and acts adolescence are the final phase of a continuous unilaterally. The effect cannot be reproduced by process of sexual differentiation that starts in early systemic injections of testosterone. For this reason one may argue that the 'duct male organizing *The Windermere Lecture given at the joint meeting of the substance' is not a common androgenic steroid. British Paediatric Association and Scottish Paediatric Society, Aviemore, 1972. However, testosterone secreted by the Leydig cells 169 Arch Dis Child: first published as 10.1136/adc.48.3.169 on 1 March 1973. Downloaded from 170 H. K. A. Visser ANDROGENIC HORMONE EXT. GENJITALIA DIFFERENTIATION 1,7OLFFIAN DUCTS (INT. GENITALIA) SUPPRESSION MtILLERIAN DUCTS IMPRINTING BRAIN EXT. GED;ITALIA NO DIFFERENTIATION WOLPFIAN DUCTS DIFFERENTIATION MULLERIAN DUCTS (INT. GENITALIA) T IMPRINTING BRAIN FIG. 1.-Schematic presentation ofprenatal sexual differentiation (adaptedfrom Prader, 1971; for explanation see text). copyright. of the fetal testis probably will be present locally 1970), oestradiol (Knorr, Kirschner, and Taylor, (around the testis) in high concentrations which 1970), and gonadotropins have been estimated in cannot be achieved by systemic injections of testo- plasma and urine of prepubertal children. Several sterone. authors have reported that prepubertal boys Inhibition of the development of the Fallopian respond to administration of human chorionic tubes and uterus from the Miillerian ducts cannot gonadotropin (HCG) for 4 to 15 days with an http://adc.bmj.com/ be accomplished by testosterone. The factor increased excretion of urinary testosterone (Loras, involved is still unknown; it certainly is not an Ollagnon, and Bertrand, 1966), or with an increase androgen. Fig. 1 summarizes these events. Only in plasma testosterone levels (Saez and Bertrand, the presence of androgens will induce the develop- 1968; Rivarola, Bergada, and Cullen, 1970). ment of male external genitalia. In the presence of Zachmann and co-workers (1971) have shown functioning fetal testes the Mullerian ducts involute, recently that even after a single dose of HCG while the Wolffian ducts develop (ductus deferens, prepubertal boys respond with an increased excre- epididymis, seminal vesicles). In the absence of tion of urinary testosterone. This procedure can on September 26, 2021 by guest. Protected testes the Wolffian ducts disappear, the Miillerian be used to study the function of the testis before structures develop (Fallopian tubes, uterus, upper puberty. Apparently, mature Leydig cells are not part of vagina). Female development of the genital required to produce testosterone in response to ducts occurs not only in the presence of an ovary, HCG. but also when no gonad is present. During recent years several studies have reported values for plasma and urinary gonadotropin con- Maturation of gonadal secretory function. centrations during childhood and pubertal develop- In the male, Leydig cells become inactive a few ment (Johanson et al., 1969; Raiti et al., 1969; weeks after birth and change into mesenchymal Rifkind et al., 1970; Lee, Midgley, and Jaffe, 1970; cells. During childhood the ovary and testis Penny et al., 1970), but until very recently little histologically show no signs of activity. However, or no information was available on plasma concen- using sensitive techniques, small amounts of testo- trations of gonadotropins and gonadal hormones sterone (Frasier and Horton, 1966; Forest and during the stages of puberty. Grumbach and co- Migeon, 1970; Degenhart, Visser, and Wilmink, workers (Burr et al., 1970; August, Grumbach, Arch Dis Child: first published as 10.1136/adc.48.3.169 on 1 March 1973. Downloaded from Some physiological and cilinicalV. aspects of1- puberty 171 PLASMA and Kaplan, 1972; Sizonenko et al., 1970; Jenner LH FSH ng/ml et al., 1972) have now published data on 30- 6- plasma 25- 5- concentrations of gonadotropins (FSH, follicle- LH stimulating hormone, and LH, luteinizing hormone) 2-0- 4- and gonadal hormones (testosterone, 17,-oestradiol) 15- 3- FSH in relation to pubertal development in the male and 10- 2- female. These results are schematically shown in 0.51 1 - Fig. 2 and 3. Though such cross-sectional studies I I I I 1 2 3 4 5 ADULT PLASMA LH FSH ng/ml PLASMA TESTOSTER(ONE 2-5-5- LH 20- 4 600 - ng/nni 500- 1 5- 3- FS 400 - 1-0- 2- _ 300- 0-5- 1- 200 - 1001 1 2 3 4 5 I.I 5I I I I I 1713 1 2 3 4 5 ADULT OESTRADIOL pg/ml STAGE OF PUBERTY 60- 8--12-13-14- 15 ADULT 50- BONE AGE (YEARS) 40- (a) 30- 20- copyright. PLASMA 10 LH FSH ng/mI 5- 25- 1 2 3 4 5 2O- 4- LH STAGE OF PUBERTY 16- 3- FSH X UNDETECTABLE < 10-] 2- 7 pg/mi 0.5- 1- FIG. 3.-Schematic presentation of changes in plasma LH, FSH, and 17fl-oestradiol during puberty in the female. http://adc.bmj.com/ 5 7 9 11 13 15 17 ADULT Vertical bars indicate periods of greatest changes. Based on data from the cross-sectional study of Jenner et al. PLASMA (1972). The curves represent our own interpretation of TESTOSTERONE the data. 600 ng/mi 500- TESTICULAR 400- VLUME /-/ have their well-known limitations and do not necessarily show the sequence of events in indivi- 300- dual boys and girls, these data are the best available on September 26, 2021 by guest. Protected 200- at this moment and certainly describe the general 100- trend in hormonal events during puberty. 5 7 9 11 13 In boys pubertal development apparently starts 15 17 ADULT with an increase in the plasma concentration of BONE AGE (YEARS) luteinizing hormone (LH). There is an increase (b) of testicular volume and an initial rise of plasma testosterone (2nd stage of puberty). Subsequently FIG. 2.-Schematic presentation of changes in plasma there is an increase in the plasma concentration of LH (luteinizing hormone), FSH (follicle-stimulating follicle-stimulating hormone (FSH). During the hormone), and testosterone during puberty in the male, 3rd to 5th stage ofpuberty there is a gradual increase related to (a) stage of puberty, (b) bone age. Vertical both and bars indicate periods of greatest changes. Based on data of LH FSH, while a sharp rise in plasma from cross-sectional studies of Burr et al. (1970) and testosterone, associated with further testicular August et al.
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